Table 2. Preclinical studies about anti-obesity effects of capsaicin.
| Treatments | Species | Duration | Metabolic disorders | Potential mechanism | Reference |
|---|---|---|---|---|---|
| 0–250 μmol/l capsaicin | 3T3-L1 preadipocytes and adipocytes | 24–72 h | Decreased the amount of intracellular triglycerides, GPDH activity | Inhibited the expression of PPARγ, C/EBP-α, and leptin | Hsu et al. [52] |
| Induced apoptosis | Induced up-regulation of adiponectin at the protein level | ||||
| Inhibited adipogenesis | |||||
| 1 μmol/l capsaicin | 3T3-L1 preadipocytes | 3–8 days | Prevented the adipogenesis | Increased intracellular calcium | Zhang et al. [53] |
| 0.015% capsaicin | Male C57BL/6 mice | 10 weeks | Decreased triglyceride levels | Decreased TRPV-1 expression in adipose tissue | Kang et al. [54] |
| Lowered fasting glucose, insulin, and leptin levels | Increased mRNA/protein of adiponectin in the adipose tissue | ||||
| Increased PPARα/PGC-1α mRNA in the liver | |||||
| 10 mg/kg body weight capsaicin | Std ddY mice | 2 weeks | Lower body weight | Increased oxygen consumption | Ohnuki et al. [55] |
| Markedly suppressed body fat accumulation | Stimulated the secretion of adrenalin | ||||
| Decreased triglyceride levels | |||||
| 0.3% capsinoids | C57BL/6J mice | 8 weeks | Suppressed body weight gain under the HFD | Increased energy expenditure | Saito et al. [57], Ohyama et al. [58] |
| Decreased plasma cholesterol level | Activation of fat oxidation in skeletal muscle | ||||
| Prevented diet-induced liver steatosis | Activation lipolysis in BAT | ||||
| Increased cAMP levels and PKA activity in BAT | |||||
| 0.003%, 0.01%, and 0.03% capsaicin | wild-type and TRPV1−/− mice | 16 weeks | Promoted weight loss | Increased the expression of UCP-1, BMP8b, SIRT-1, PGC-1α, and PRDM-16 in BAT | Baskaran et al. [59] |
| Enhanced the respiratory exchange ratio | Increased the phosphorylation of SIRT-1 | ||||
| Countered hypercholesterolemia | |||||
| 0.01% capsaicin | wild-type and TRPV1−/− mice | 26 weeks | Countered obesity | Promoted SIRT-1 expression | Baskaran et al. [60] |
| Browning of WAT | Increased the expression of PGC-1α | ||||
| Facilitated PPARγ–PRDM-16 interaction | |||||
| 0.01% capsaicin | wild-type and TRPV1−/− mice | 24 weeks | Ameliorated abnormal glucose homeostasis | Activation of TRPV1-mediated GLP-1 secretion in the intestinal cells | Wang et al. [49] |
| Increased GLP-1 levels in the plasma and ileum | |||||
| 640 μmol/L, 2 ml/kg capsaicin | Sprague-Dawley rats | 15 min | Increased superior mesenteric artery blood flow | Induced a dichotomous pattern of blood flow changes | Leung et al. [68] |
| Reduction in hydrogen gas clearance | |||||
| 0.01% capsaicin | C57BL/6J male mice | 9 weeks | Reduced weight gain | Modest modulation of the gut microbiota | Shen et al. [69] |
| Improved glucose tolerance | Up-regulated the expression of Muc2 and antimicrobial protein gene Reg3g in the intestine |
BMP8b, bone morphogenetic protein-8b; cAMP, cyclic adenosine monophosphate; C/EBP-α, CCAAT-enhancer-binding protein-α; GPDH, glycerol-3-phosphate dehydrogenase; Muc2, mucin 2 gene; PGC1-α, PPARγ co-activator 1-α; PKA, protein kinase A; PRDM-16, positive regulatory domain containing 16; Reg3g, regenerating islet-derived protein 3γ; SIRT-1, sirtuin-1; UCP-1, uncoupling protein 1; WAT, white adipose tissue.